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Abstract BACKGROUND Traumatic brain injury (TBI) remains one of the most challenging health and socioeconomic problems of our times. Clinical courses may be complicated by hemostatic abnormalities either pre-existing or developing with TBI. OBJECTIVE To review frequencies, patterns, mechanisms, novel approaches to diagnostics, treatment, and outcomes of hemorrhagic progression and coagulopathy after TBI. METHODS Selective review of the literature in the databases Medline (PubMed) and Cochrane Reviews using different combinations of the relevant search terms was conducted. RESULTS Of the patients, 20% with isolated TBI display laboratory coagulopathy upon hospital admission with profound effect on morbidity and mortality. Preinjury use of antithrombotic agents may be associated with higher rates of hemorrhagic progression and delayed traumatic intracranial hemorrhage. Further testing may display various changes affecting platelet function/numbers, pro- and/or anticoagulant factors, and fibrinolysis as well as interactions between brain tissues, vascular endothelium, mechanisms of inflammation, and blood flow dynamics. The nature of hemostatic disruptions after TBI remains elusive but current evidence suggests the presence of both a hyper- and hypocoagulable state with possible overlap and lack of distinction between phases and states. More “global” hemostatic assays, eg, viscoelastic and thrombin generation tests, may provide more detailed and timely information on the overall hemostatic potential thereby allowing early “goal-directed” therapies. CONCLUSION Whether timely and targeted management of hemostatic abnormalities after TBI can protect against secondary brain injury and thereby improve outcomes remains elusive. Innovative technologies for diagnostics and monitoring offer windows of opportunities for precision medicine approaches to managing TBI.

The association between coagulopathy and either isolated traumatic brain injury (TBI) or progressive hemorrhagic injury (PHI) remains controversial. The aims of this study were to evaluate whether isolated TBI induces pronounced coagulopathy, in comparison with non-TBI or TBI in conjunction with other injuries (TBI + other injuries), and to examine whether there is any evidence of a relationship between coagulopathy and PHI in patients who have experienced TBI. The MEDLINE® and Embase databases, and the Cochrane Central Register of Controlled Trials (Central), were trawled for relevant studies. Searches covered the period from the inception of each of the databases to June 2015, and were conducted using appropriate combinations of terms and key words based on medical subject headings (MeSH). Studies were included if they compared isolated TBI with a similar severity of injury to other body regions, or compared PHI with non-PHI, with regard to coagulation tests and the prevalence of coagulopathy. We extracted the means and standard deviations (SD) of coagulation test levels, as well as their ranges or the percentage of abnormal coagulation tests, in both cases and controls. A total of 19 studies were included in our systematic review and meta-analysis. Only the mean fibrinogen (FIB) in isolated TBI was found to be significantly higher than in TBI + other injuries (pooled mean difference [MD] 32.09; 95% confidence interval [CI] 4.92–59.25; p = 0.02); in contrast, it was also significantly higher than in non-TBI (pooled MD 15.44; 95% CI 0.28–30.59; p = 0.05). We identified 15 studies that compared coagulopathy between a PHI group and a non-PHI group. The PHI group had a lower platelet count (PLT) value (pooled MD −19.21; 95% CI: −26.99 to −11.44, p < 0.001) and a higher international normalized ratio (INR) value (pooled MD 0.07; 95% CI: 0.02–0.13, p = 0.006) than the non-PHI group, but no differences were observed in the mean activated partial thromboplastin time (APTT) and prothrombin time (PT) between the PHI and non-PHI patients. In addition, PHI was significantly associated with a higher percentage of INR >1.2 (pooled OR 3.49 [95% CI 1.97–6.20], p < 0.001), PLT <100 × 109/L (pooled OR 4.74 [95% CI 2.44–9.20], p < 0.001), and coagulopathy (pooled OR 2.52; 95% CI 1.88– 3.38; p < 0.001), compared with non-PHI. The current clinical evidence does not indicate that the prevalence of coagulopathy in TBI is significantly higher than in injuries of similar severity to other areas of the body, or in multiple injuries with TBI. With respect to the association between coagulopathy and PHI, the occurrence of coagulopathy, INR, and PLT was significantly associated with PHI, but APTT and PT were not found to be associated with PHI. In the future, high quality research will be required to further characterize the effects of coagulopathy on TBI and subsequent PHI.

s Background The extent of psychiatric disorders after head injury is not well recognized. We assessed the prevalence and treatment of psychiatric disorders after traumatic intracranial hemorrhage (tICH) in a 10-year follow-up. Methods An observational, retrospective single-center cohort of tICH patients from HEAD Helsinki (Head trauma related health care Economics, Acute care and Development of long-term outcomes in Helsinki city region) study hospitalized at Helsinki University Hospital between 01 January and 31 December 2010. We reported primary outcomes as psychiatric disorders and their subsequent treatment on secondary level psychiatric care during the follow-up period between January 2010 and December 2019. Logistic regression analysis was performed to study associations between admission clinical characteristics and primary outcomes. Results In our cohort of 385 patients (mean age 60.7 years, 66.5% male) with tICH, 66 (17.1%) had any psychiatric disorders during the follow-up period (median time 108 months, IQR 92 months), and 48 (72.1%) of them experienced new psychiatric disorders (median time to onset 29.5 months, IQR 64 months), of which 26 (54.2%) were without any psychiatric history prior to tICH. A total of 35 patients (53.0%) received secondary level psychiatric care, and 40 (60.6%) patients had initiated new psychotropics (median time to initiation 8 months, IQR 40 months). Compared to patients without psychiatric disorders, those with psychiatric disorders were younger (mean age 49.1 vs. 63.1 years, p  < 0.001) and had less frequently larger (> 100 ml) intracranial hemorrhages (21.2 vs. 44.2%, p  = 0.001). In multivariable analyses, younger age was independently associated with the development of any psychiatric disorders. Prior psychiatric medication and lower admission GCS score were associated with consequent psychiatric treatment. Conclusions Every sixth patient treated in a tertiary level neurosurgical unit had psychiatric disorders diagnosed at secondary level care after tICH and over half of them received secondary level psychiatric care. Psychiatric disorders development was associated with younger age whereas prior psychiatric medication and lower admission GCS score indicated subsequent psychiatric treatment.

Pre-injury anti-platelet use has been associated with increased risk of progression of traumatic intracranial hemorrhage (TICH) and worse outcomes. VerifyNow® assays assess platelet inhibition due to aspirin/clopidogrel. This study assesses the outcomes of patients with TICH and platelet dysfunction treated with desmopressin and/or platelets. We performed a retrospective chart review of patients with mild TICH at a level 1 trauma center 1/1/2013–6/1/2016. Patients with documented platelet dysfunction who received desmopressin and/or platelets were compared to those who were untreated. Primary outcomes were progression of TICH and neurologic outcomes at discharge. Of 565 patients with a mild TICH, 200 patients had evidence of platelet dysfunction (a positive VerifyNow® assay). Patients had similar baseline demographics, injury characteristics, and rate of TICH progression; but patients who received desmopressin and/or platelets had worse Glasgow Outcomes Score at discharge. Treatment of patients with mild TICH and platelet dysfunction with desmopressin and/or platelets did not affect TICH progression but correlated with worse neurologic status at discharge. [Display omitted] •Traumatic brain injury patients may have worse outcomes if on antiplatelet therapy.•Treating these patients with desmopressin and/or platelets may not improve outcomes.•Further studies to investigate optimal treatment strategies for these patients are warranted.

Background The role of coagulopathy in patients with traumatic brain injury has remained elusive. In the present study, we aim to assess the prevalence of coagulopathy in patients with traumatic intracranial hemorrhage, their clinical features, and the effect of coagulopathy on treatment and mortality. Methods An observational, retrospective single-center cohort of consecutive patients with traumatic intracranial hemorrhage treated at Helsinki University Hospital between 01 January and 31 December 2010. We compared clinical and radiological parameters in patients with and without coagulopathy defined as drug- or disease-induced, i.e., antiplatelet or anticoagulant medication at a therapeutic dose, thrombocytopenia (platelet count < 100 E9/L), international normalized ratio > 1.2, or thromboplastin time < 60%. Primary outcome was 30-day all-cause mortality. Logistic regression analysis allowed to assess for factors associated with coagulopathy and mortality. Results Of our 505 patients (median age 61 years, 65.5% male), 206 (40.8%) had coagulopathy. Compared to non-coagulopathy patients, coagulopathy patients had larger hemorrhage volumes (mean 140.0 mL vs. 98.4 mL, p < 0.001) and higher 30-day mortality (18.9% vs. 9.7%, p = 0.003). In multivariable analysis, older age, lower admission Glasgow Coma Scale score, larger hemorrhage volume, and conservative treatment were independently associated with mortality. Surgical treatment was associated with lower mortality in both patients with and without coagulopathy. Conclusions Coagulopathy was more frequent in patients with traumatic intracranial hemorrhage presenting larger hemorrhage volumes compared to non-coagulopathy patients but was not independently associated with higher 30-day mortality. Hematoma evacuation, in turn, was associated with lower mortality irrespective of coagulopathy.

After a traumatic intracranial hemorrhage (tICH), patients often receive a platelet transfusion to reverse the effects of antiplatelet medication and to reduce neurologic complications. As platelet transfusions have their own risks, this study evaluated their effects on tICH progression, need for operations and mortality. In this retrospective study, we identified patients admitted to a level 1 trauma centre with a tICH from 2011 to 2015 who were taking acetylsalicylic acid (ASA) or clopidogrel, or both. We categorized patients into 2 groups: platelet transfusion recipients and nonrecipients. We collected data on demographic characteristics, changes in brain computed tomography findings, neurosurgical interventions, in-hospital death and intensive care unit (ICU) length of stay (LOS). We used multivariable logistic regression to compare outcomes between the 2 groups. We identified 224 patients with tICH, 156 (69.6%) in the platelet transfusion group and 68 (30.4%) in the no transfusion group. There were no between-group differences in progression of bleeds or rates of neurosurgical interventions. In the transfusion recipients, there was a trend toward increased ICU LOS (adjusted odds ratio [OR] 1.59, 95% confidence interval [CI] 0.74–3.40) and in-hospital death (adjusted OR 3.23, 95% CI 0.48–21.74). There were no differences in outcomes between patients who received platelet transfusions and those who did not; however, the results suggest a worse clinical course, as indicated by greater ICU LOS and mortality, in the transfusion recipients. Routine platelet transfusion may not be warranted in patients taking ASA or clopidogrel who experience a tICH, as it may increase ICU LOS and mortality risk. Après une hémorragie intracrânienne traumatique, les patients reçoivent souvent une transfusion de plaquettes pour inverser les effets des médicaments antiplaquettaires et réduire les complications neurologiques. Les transfusions de plaquettes comportent des risques particuliers; l’étude portait sur leurs effets sur la progression de l’hémorragie intracrânienne traumatique, ainsi que sur la nécessité d’une opération et la mortalité. Dans cette étude rétrospective, nous avons ciblé des patients atteints d’une hémorragie intracrânienne traumatique admis dans un centre de traumatologie de niveau 1, de 2011 à 2015, qui prenaient de l’acide acétylsalicylique (AAS) ou du clopidogrel, ou les deux. Ces patients ont été classés en 2 catégories : ceux ayant reçu une transfusion de plaquettes et ceux n’ayant pas reçu de transfusion. Nous avons recueilli des données sur les caractéristiques démographiques, les changements des résultats de la tomodensitométrie cérébrale, les interventions neurochirurgicales, les décès à l’hôpital et la durée de séjour en unité de soins intensifs. Nous avons eu recours à une analyse de régression logistique multivariée pour comparer les résultats entre les 2 groupes. Nous avons ciblé 224 patients atteints d’une hémorragie intracrânienne traumatique : 156 (69,6 %) ayant reçu une transfusion de plaquettes et 68 (30,4 %) n’ayant pas reçu de transfusion. Il n’y avait aucune différence entre les groupes concernant la progression des saignements ou les taux d’interventions neurochirurgicales. Chez les patients ayant reçu une transfusion, on a observé une tendance à la hausse de la durée de séjour en unité de soins intensifs (rapport de cotes [RC] ajusté de 1,59; intervalle de confiance [IC] de 95 %, 0,74–3,40) et des décès à l’hôpital (RC ajusté de 3,23; IC de 95 % de 0,48–21,74). On n’a observé aucune différence au chapitre des résultats entre les patients ayant reçu une transfusion de plaquettes et les autres. Toutefois, les résultats suggèrent une évolution clinique défavorable chez les patients ayant reçu une transfusion, se traduisant par une durée de séjour en unité de soins intensifs plus longue et un taux de mortalité plus élevé. La transfusion plaquettaire systématique pourrait ne pas être avisée chez les patients prenant de l’AAS ou du clopidogrel qui souffrent d’une hémorragie intracrânienne traumatique, car elle pourrait faire augmenter la durée de séjour en unité de soins intensifs et exacerber le risque de mortalité.

BackgroundSeveral current guidelines do not include antiplatelet use as an explicit indication for CT scan of the head following head injury. The impact of individual antiplatelet agent use on rates of intracranial haemorrhage is unclear. The primary objective of this systematic review was to assess if clopidogrel monotherapy was associated with traumatic intracranial haemorrhage (tICH) on CT of the head within 24 hours of presentation following head trauma compared with no antithrombotic controls.MethodsEligible studies were non-randomised studies with participants aged ≥18 years old with head injury. Studies had to have conducted CT of the head within 24 hours of presentation and contain a no antithrombotic control group and a clopidogrel monotherapy group.Eight databases were searched from inception to December 2020. Assessment of identified studies against inclusion criteria and data extraction were carried out independently and in duplicate by two authors.Quality assessment and risk of bias (ROB) were assessed using the Newcastle–Ottawa Quality Assessment tool and Risk Of Bias In Non-randomised Studies of Interventions (ROBINS-I) tool. Meta-analysis was conducted using a random-effects model and reported as an OR and 95% CI.ResultsSeven studies were eligible for inclusion with a total of 21 898 participants that were incorporated into the meta-analysis. Five studies were retrospective. Clopidogrel monotherapy was not significantly associated with an increase in risk of tICH compared with no antithrombotic controls (OR 0.97, 95% CI 0.54 to 1.75). Heterogeneity was high with an I2 of 75%. Sensitivity analysis produced an I2 of 21% and did not show a significant association between clopidogrel monotherapy and risk of tICH (OR 1.16, 95% CI 0.87 to 1.55). All studies scored for moderate to serious ROB on categories in the ROBINS-I tool.ConclusionIncluded studies were vulnerable to confounding and several were small-scale studies. The results should be interpreted with caution given the ROB identified. This study does not provide statistically significant evidence that clopidogrel monotherapy patients are at increased risk of tICH after head injury compared with no antithrombotic controls.PROSPERO registration numberCRD42020223541.

Traumatic intracranial hemorrhage (TICH) patients with acute kidney injury (AKI) were reported to have a high mortality rate. Renal replacement therapy (RRT) is indicated for patients with a severe kidney injury. This study aimed to compare the effects of different RRT modalities regarding chronic dialysis rate among adult TICH patients with AKI. A retrospective search of computerized hospital records from 2000 to 2010 for patients with a discharge diagnosis of TICH was conducted to identify the index cases. We collected the data of TICH patients with increased intracranial pressure combined with severe AKI who received intermittent hemodialysis (IHD) or continuous veno-venous hemofiltration (CVVH) as RRT. The outcome was dialysis dependence between 2000 and 2010. From a total of 310 patients who were enrolled in the study, 134 (43%) received CVVH and 176 (57%) received IHD. The risk of dialysis dependency was significantly lower in the CVVH group than in the IHD group (adjusted hazard ratio: 0.368, 95% CI, 0.158-0.858, P = 0.034). Diabetes mellitus and coronary artery disease were risk factors for dialysis dependency. CVVH compared with IHD modality was associated with lower dialysis dependency rate in TICH patients combined with AKI and diabetes mellitus and those with an injury severity score (ISS) ≥16. CVVH may yield better renal outcomes than IHD among TICH patients with AKI, especially those with diabetes mellitus and an ISS ≥16. The beneficial impact of CVVH on TICH patients needs to be clarified in a large cohort study in future.

Venous thromboembolism is a common complication of traumatic brain injury with an estimated incidence of 25% when chemoprophylaxis is delayed. The timing of initiating prophylaxis is controversial given the concern for hemorrhage expansion. To determine the safety of initiating venous thromboembolic event (VTE) chemoprophylaxis within 24 h of presentation. We performed a retrospective analysis of patients with traumatic intracranial hemorrhage presenting to a level I trauma center. Patients receiving early chemoprophylaxis (<24 h) were compared to the matched cohort of patients who received heparin in a delayed fashion (>48 h). The primary outcome of the study was radiographic expansion of the intracranial hemorrhage. Secondary outcomes included VTE, use of intracranial pressure (ICP) monitoring, delayed decompressive surgery, and all-cause mortality. Of 282 patients, 94 (33%) received chemoprophylaxis within 24 h of admission. The cohorts were evenly matched across all variables. The primary outcome occurred in 18% of patients in the early cohort compared to 17% in the delayed cohort (P = .83). Fifteen patients (16%) in the early cohort underwent an invasive procedure in a delayed fashion; this compares to 35 patients (19%) in the delayed cohort (P = .38). Five patients (1.7%) in our study had a VTE during their hospitalization; 2 of these patients received early chemoprophylaxis (P = .75). The rate of mortality from all causes was similar in both groups. Early (<24 h) initiation of VTE chemoprophylaxis in patients with traumatic intracranial hemorrhage appears to be safe. Further prospective studies are needed to validate this finding.

Traumatic brain injury (TBI) is the leading cause of pediatric morbidity and mortality worldwide, and half of all fatalities occur in infants aged less than 1 year. We analyzed 129 infants diagnosed with TBI complicated with intracranial hemorrhage confirmed by brain computed tomography. We defined delta hemoglobin (ΔHB) as nadir HB - age specific mean HB, and the ratio of HB (%) as ΔHB/age specific mean HB x 100. Infants with poor neurologic outcomes had a lower admission HB and ΔHB (p < 0.05). The in-hospital mortality rate was 10.1% (13 infants), and the infants who died had a significantly lower ΔHB ratio compared to the survivors. The area under the receiving operating characteristic curve (AUC) of initial Glasgow Coma Score (GCS) in predicting neurologic outcomes was higher than that of ratio of ΔHB (0.881 v.s 0.859). In multivariate logistic regression analysis with the optimal cutoff ratio of ΔHB, it remained an independent predictor for in-hospital mortality and poor neurologic outcomes at discharge and at 6 months. AUC analysis for the ratio of ΔHB for poor neurologic outcomes in infants aged from 0–6 months was 0.85 and the optimal cutoff was −30.7% (sensitivity, 69%; specificity, 92%; positive likelihood ratio (LR + ), 8.24; negative likelihood ratio (LR − ), 0.34); the AUC was 0.88 in infants aged from 6–12 months and the optimal cutoff was −20.6% (sensitivity, 89%; specificity, 79%; LR + , 4.13; LR − , 0.15).